SHOCK IN OBSTETRICS &

GYNECOLOGY
DR. ABDUL-RAZAK S. ABDUL-
MUMIN
 DEFINITION
Generalised circulatory failure
characterised by inadequate tissue
perfusion
Compromised tissue perfusion that
causes cellular hypoxia and vital
organ dysfunction
Insufficient perfusion to meet
metabolic demands of tissues
leading to cellular hypoxia and end
organ damage
 PHASES/STAGES
(COMPENSATED, PROGRESSIVE, IRREVERSIBLE)

COMPENSATED 0R NON-PROGRESSIVE
Reduced blood volume leads to reduced
cardiac output resulting in falling arterial
Stimulates sympathetic nervous system
thro baroreceptors.
Increased vasoconstriction of arterioles,
peripheral vascular resistance, venous
return, cardiac output and heart rate
increases, mean arterial rises, preventing
further deterioration
 COMPENSATED
Renin-angiotensin system causes
vasoconstriction in the renal,
gastrointestinal & other organs to
divert blood to heart and brain
Anti diuretic hormone is released and
acts to conserve fluid loss thro the
kidneys
If the cause is not reversed shock
enters progressive stage
 PROGRESSIVE
Continuous blood loss further decreases
arterial and results in poor coronary flow
The myocardium weakens worsening the
cardiac output
A cycle of progressive cardiac
deterioration develops.
The compensatory mechanism begins to
fail
Na+ build up in cells whist K+ leaks out
 PROGRESSIVE
Lack of O2 results in anaerobic
metabolism with continuous build up
of metabolic acidosis
Pre-capillary sphincters and arteriolar
smooth muscles relax and blood
accumulates in the capillaries
Capillary hypoxia causes increased
capillary permeability and fluid loss
into extra cellular space worsening
the shock
 IRREVERSIBLE
Vital organs like kidneys have failed
and shock can no longer be reversed
Brain damage occurs and death occurs
immediately
Tissue damage is due depletion of high
energy phosphate compounds
Cellular ATP degraded to ADP, AMP and
adenosine due to lack of O2 in the
mitochondria
 IRREVERSIBLE
Adenosine diffuses out of cells and is
converted into uric acid which cannot
reenter the cell
New high energy compounds are
difficult to regenerate during this
final stage irreversible shock.
 TYPES/CLASSIFICATION
HYPOVOLEMIC SHOCK
CARDIOGENIC SHOCK
DISTRIBUTIVE/VASOGENIC SHOCK:-
(SEPTIC, ANAPHYLACTIC,
NEUROGENIC)
 HYPOVOLEMIC SHOCK
Insufficient circulatory volume as a result of
blood or fluid loss. Burns, diarrhoea, blood
loss, intestinal obstruction
Causes in OBGYN mostly hemorrhagic from
acute blood loss
OBSTETRICS
EARLY PREGNANCY; Ruptured ectopic
pregnancy, inevitable and incomplete
abortions, gestational trophoblastic disease
 HYPOVOLEMIC
(hemorrhagic)
LATE PREGNANCY; placenta previa,
placental abruption, pre-
eclampsia/eclampsia (liver
subcapsullar hemorrhage)
DELIVERY & PUERPERIUM; ruptured
uterus, C/S, APH, uterine inversion,
PPH( uterine atony, retained products
& placenta, genital tract laceration),
placenta accreta
 HYPOVOLEMIC
(GYNECOLOGY)
Genital tract trauma (falling astride
with vulva hematoma, coital
laceration), bleeding fibroids,
abnormal menstruation with
excessive flow, genital tract
malignancies, following surgeries,
ovarian torsion, ruptured ovarian
cyst (corpus luteal)
 CARDIOGENIC
Failure of heart to pump effectively.
This may be due to
Cardiac diseases pre dating the
pregnancy (heart valve problems),
cardiac events during pregnancy like
Myocardial infarction,
cardiomyopathies, CCF, cardiac
tamponade, pulmonary embolism,
 DISTRIBUTIVE/VASOGENIC
(septic, anaphylactic, neurogenic)
Impaired utilisation of O2 and energy
production by cells
SEPTIC SHOCK
Overwhelming infection usually gram
negative bacteria
Production of endotoxins initiating
inflammatory response causing
vasodilatation, endothelial damage and
lowering peripheral vascular resistance and
hypotension
 SEPTIC SHOCK
Increased capillary permeability, leakage
of fluid into the extra vascular space
Poorly distributed blood flow resulting in
inadequate tissue perfusion
Causes in OBGYN septic incomplete
abortions, chorioamnionitis, puerperal
sepsis, unsafe abortion, tubo ovarian
abscess, pelvic infection, pyelonephritis,
toxic shock syndrome
 ANAPHYLACTIC SHOCK
Anaphylaxis provoked by antigen,
allergen
Results in histamine release, then
vasodilatation, increased capillary
permeability and hypotension
Examples in OBGYN, transfusion of
inadvertent/wrong cross matched
blood
 SIGNS & SYMPTOMS
HYPOVOLEMIC SHOCK
Rapid weak pulse
Cold clammy
skin/peripheries( peripheral
vasoconstriction)
Rapid shallow breathing
Dry mouth and lips
Low blood pressure
 CARDIOGENIC
Distended jugular veins
Weak or absent pulse
Arrhythmia, tachycardia
Pulsus paradoxicus (cardiac
tamponade)
DISTRIBUTIVE (septic shock)
Fever, chills
Warm peripheries, hypotension
Tachycardia, weak pulse then
peripheries become cold
Mental confusion
cyanosis
 MANAGEMENT
Patient survival depends on
Prompt assessment(severity, cause) and
treatment in order to prevent shock
becoming irreversible
Patient must be stabilised before definitive
treatment is offered (not necessarily fully
stable)
Definitive treatment; medical, surgery or both
Must be a team based approach to
management
 MANAGEMENT
Intravenous access with a wide bore
cannula
Full blood count
Blood for grouping & cross matching
Coagulation studies prothrombin
time, partial thromboplastin time,
fibrinogen, platelet count
Arterial blood gases
Serum biochemistry, electrolytes,
glucose
 MANAGEMENT
ECG
Chest X-ray
Cultures of specimen including blood,
endocervix, etc
Volume replacement with crystalloids whilst
waiting for blood
O 2 administration, intra nasal, or by
intubation
Indwelling urethral catheter to monitor urine
output
 MANAGEMENT
Insert central venous line to monitor
fluid replacement(hemodynamic
evaluation)
Give sodium bicarbonate in the
presence of metabolic acidosis
Broad spectrum antibiotics whilst
waiting for C/S results (septic shock)
Treatment of underlying cause;
uterine evacuation, salpingectomy,
 MANAGEMENT
C/S or immediate delivery for APH,
placental removal, suturing of
lacerations, laparotomy for ruptured
uterus, or pelvic abscess
AMNIOTIC FLUID EMBOLISM
Rare catastrophe occurs at 1 case per 20-
30,000 deliveries, but high maternal
mortality
Can occur at any time during pregnancy,
labour/delivery or postpartum
Unpredictable and unpreventable
Risk factors include advanced maternal age,
precipitous labour, C/S, conditions
associated with bleeding in pregnancy,
uterine manipulation
AMNIOTIC FLUID EMBOLISM
Pathophysiology; result from maternal
anaphylactic reaction to fetal material
entering the pulmonary circulation
Provoking sudden pulmonary
vasoconstriction, pulmonary hypertension,
Rt. side heart failure ff by
Lt heart failure, endothelial activation and
leakage and bleeding probably due to
hypoxia, & release of injury associated
agents in the serum
AMNIOTIC FLUID EMBOLISM
Severe chest pain and
breathlessness
Bradycardia, hypotension, apnea,
coagulopathy; bleeding from the
uterus, puncture sites, seizures
Respiratory distress, cyanosis,
pulmonary edema, shock, loss of
consciousness, seizures
No standard confirmatory test for
diagnosis
 AMNIOTIC FLUID EMBOLISM
Treatment is Supportive (in ICU)
Secure airway by intubating and give oxygen
Cardiopulmonary resuscitation (CPR)
Give crystalloids and blood/blood products
with pressor agents to maintain BP
Pressor agents like dopamine etc
Central venous pressure monitoring
Treatment of coagulopathy and uterine atony
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